Marburg Virus
Introduction
Marburg virus refers to virus of the genus marbugvirus. The virus usually causes the Marburg Hemorrhagic Fever. The virus is said to have originated from Africa and specifically Central and East Africa. The virus got its name from the place where the first outbreak was discovered, Marburg in German. The virus infects both human beings and other animals, especially nonhuman primates.
The virus usually lives in the animals hosts, and human being can easily contact the virus from the animals. After the initial transmission of the virus to human beings, the virus can be transmitted among the human beings through needles that are contaminated, or through contact of other body fluids (Gerlier, 2011). No drug yet has been developed to treat the virus, but it is believed that scientist are getting closer to coming up with a vaccine, that will help deal with this deadly virus.
Marburg Virus Entry into the Cell
Marburg virus is a member of the Filoviridae family, which are usually elongated filamentous molecules that usually vary in length. The virus entry into a cell is an essential process in the life of a virus. Researchers have described the entry as a potential target for therapy. This is because if this step can be successfully inhibited, it denies the virus an opportunity for further development (Emily & Kartik, 2012). The virus can replicate in various tissues in human cells and other animals. Marburg viruses are believed to enter into the cell of the host through endocytosis process, which is usually aided by the receptor. Its replication process starts when the virus enters into the human cell. The process of entry mainly involves various steps. These steps start with the virus binding to the receptor. Later, with the help of various attachment factors, the virus then goes through viral fusion process, penetrates nucleoplasm of the cell and finally reaches the cytoplasm.
A protein that is usually on its surface facilitates the binding of the virus. This protein is known as the filoviral glycoprotein or simply GP. The protein assists the virus to not only bind, but also in the fusion of the virus envelope with the cell membrane. GP is a viral membrane fusion glycoprotein class I and usually resemble the prototypic HIV-1. A mature GP usually divides into GP1 and GP2. GP 1 protein helps in interactions that occur between the virus and its receptor (Emily & Kartik, 2012). These viruses also have the ability to enter and infect numerous cells. The virus usually displays a wide mammalian host cell range. This suggests that the virus usually requires one cell surface receptor.
Figure 1: Marburg virus entry into the cell
Another important unique characteristic in the entry of the virus is that they usually use chemical inhibitors, to block any other cell from synthesizing them. These chemical inhibitors include clathrin and macropinoctic (Emily & Kartik, 2012). The virus usually uses these chemicals inhibitors in their pathways. Studies have also shown that there are other cytolistic factors that also aids in the entry of the Marburg viruses
Marburg Virus Replication
Although it is well known that Marburg virus replicates in numerous tissues and cell types, the molecular process of their broad tropism is not yet clearly explained or understood. The lifecycle of a Marburg virus starts with the virus attaching in to the cell receptor. This is usually followed by the fusion of the virus envelops with the cellular coat of the receptor (Harty, 2008). It is after this that the virus usually removes the upper coat of the nucleoplasid. The virus later transcribes its gene into mRNAs, which are positive stranded. The mRNAs are then translated into other structural and non-structural proteins.
After translation, soluble form of GP are formed as a result of failure to form disulphide bonds between the natural forms of the GP that is GP1 and GP2. The role of these two GP forms is not yet clear. Transcription of the negative RNA by the polymerase complex of the virus results into mRNAs, which are later translated into ribosome (Gerlier, 2011). During the replication process, the positive senses of the viral genome are produced. These later acts as the templates that are used in synthesize of the viral genome.
Figure 2: Marburg virus replication
Replication of the Marburg virus usually yields into full-elongated positive antigenomes, which are later transcribed into copies of progeny genome of the same virus. The newly formed protein and genomes later join at the inner side of the cell membrane. The virions are then detached from the cell, after which they are able to get new coatings from the cellular membrane that they detach from (Emily & Kartik, 2012). The mature virions later infect the other new cells, and they repeat the cycle of replication again.
Conclusion
Marburg virus entry and replication inside human bodies is not yet clear. This is because the after the virus enters the human body it takes a very short time for it to replicate and attack almost all the body cells. This gives the reason behind why the virus is highly contagious and easily spread from one person to the other in a very short time.
Reference list
Emily, H. M., & Kartik, C. (2012). Filovirus entry into cells – new insights. Current Opinion in Virology, 2 (2), 206-214.
Gerlier, D. (2011). Emerging zoonotic viruses: new lessons on receptor and entry mechanisms. Current Opinion in Virology, 1 (1), 27-34.
Harty, R. N. (2008). Review: No exit: Targeting the budding process to inhibit filovirus replication. Antiviral Research, 81 (3), 189-197.
